Oncotarget

Research Papers:

Effect of PGE2-EPs pathway on primary cultured rat neuron injury caused by aluminum

Lu Yang, Yuling Wei, Ying Luo, Qunfang Yang, Huan Li, Congli Hu, Yang Yang and Junqing Yang _

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Oncotarget. 2017; 8:92004-92017. https://doi.org/10.18632/oncotarget.21122

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Abstract

Lu Yang1,*, Yuling Wei1,*, Ying Luo1, Qunfang Yang1, Huan Li1, Congli Hu1, Yang Yang1 and Junqing Yang1

1Department of Pharmacology, Chongqing Medical University, The Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing 400016, China

*Co-first authors

Correspondence to:

Junqing Yang, email: [email protected], [email protected]

Keywords: aluminum overload, hippocampal neuron, PGE2, PGE2 receptor

Received: July 04, 2017     Accepted: September 03, 2017     Published: September 21, 2017

ABSTRACT

To observe the characteristic changes of PGE2-EPs pathway and divergent functions of PGE2 receptor subtypes on neuronal injury. The primary cultured rat hippocampus neuron injury model was established via aluminum maltolate (100 μM). The aluminum-overload neurons were treated with the agonists of EP1 (17-phenyl trinor Prostaglandin E2 ethyl amide), EP2 (Butaprost), EP3 (Sulprostone) and EP4 (CAY10598) and antagonists of EP1 (SC-19220), EP2 (AH6809) and EP4 (L-161982) at different concentrations, respectively. The neuronal viability, lactate dehydrogenase leakage rate and PGE2 content were detected by MTT assay, lactate dehydrogenase assay kit and enzyme-linked immunosorbent assay, respectively. The mRNA and protein expressions of mPGES-1 and EPs were determined by RT-PCR and western blot, respectively. The pathomorphology was identified by hematoxylin-eosin staining. In the model group, neuronal viability significantly decreased, while lactate dehydrogenase leakage rate and PGE2 content increased. The mPGES-1, EP1, EP2 and EP4 mRNA expression, and the mPGES-1, EP1 and EP2 protein expression increased, while EP3 level decreased. EP3 agonist exerted protective function in neuronal viability and lactate dehydrogenase leakage rate, while EP1 agonist, EP2 and EP4 antagonist exerted an opposite effect. In conclusion, aluminum-overload caused an imbalance of PGE2-EP1-4 pathway and activation of EP receptor may provide a viable therapeutic target in neuronal injury.


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